Baicalin protects sertoli cells from heat stress-induced apoptosis via activation of the Fas/FasL pathway and Hsp72 expression

•Heat stress (HS) induced apoptosis and increased Hsp72 expression in calf sertoli cells (SCs).•HS induced apoptosis of the SCs by cleaved caspase 3 through activating Fas/FasL pathway.•Baicalin decreased apoptotic rate of the SCs treated with HS.•Baicalin decreased Fas, FasL, caspase 8 and caspase 3 expressions and increased Hsp72 expression in heat-stressed SCs.

Certain Chinese herbal medicines have antipyretic effects in both animal and human clinical practice. However, no report indicates their antipyretic effects on heat-stressed cells. The present study aimed to identify the protective effects of baicalin on the apoptosis of primary cultured bovine sertoli cells (SCs) subjected to heat stress (HS). The results demonstrated that HS induced apoptosis in the SCs exposed to 43 °C for 1 h as Fas/FasL was activated and caspase-3 was cleaved, the cells apoptotic rate was decreased. Moreover, the mRNA and protein levels of Hsp72 increased, whereas the cells apoptotic rate and expression of Fas, FasL, caspases 8 and 3 decreased in the SCs pretreated with various concentrations (0.1, 1, 10, 20 μg/mL) of baicalin prior to HS. In conclusion, baicalin ameliorates heat stress-induced cell apoptosis via the modulation of the cell survival rate through Fas/FasL pathway activation and the upregulation of Hsp72 expression in bovine SCs.

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